Food Environment Framed as Structural Driver of Cardiometabolic Risk

A neighborhood can quietly shape the heart long before a patient ever reaches a clinic. That is the central argument of a narrative review published in Frontiers in Nutrition, in which researchers from institutions including NYC Health + Hospitals/Elmhurst, Houston Methodist DeBakey Heart & Vascular Center, Case Western Reserve University, and the University of Glasgow argue that the food environment deserves recognition as a major structural component of the cardiometabolic exposome. The exposome framework, which considers cumulative environmental exposures across the life course, has already absorbed air pollution, green space, and socioeconomic conditions as recognized drivers of cardiovascular risk. The authors contend that the food environment, defined as the consumer’s interface with the food system, remains comparatively fragmented in how it is measured and interpreted, and they set out to consolidate its determinants, mechanisms, and interactions with other environmental hazards.

The review organizes the food environment around four interacting dimensions: availability, accessibility, affordability, and acceptability. Availability describes whether food vendors or products exist in a given context, whether in wild, cultivated, or built food environments. Accessibility extends this to what an individual can actually reach, incorporating distance, travel time, transportation options, physical mobility, safety, and store hours. Affordability reflects the intersection of food prices with household purchasing power, while acceptability captures whether available foods align with cultural preferences, social norms, religious restrictions, and perceived quality and safety. When food is not consistently available, accessible, affordable, or acceptable, households may experience food insecurity, which the U.S. Department of Agriculture classifies along a continuum from low food security, marked by reduced diet quality, to very low food security, marked by disrupted eating patterns and reduced intake.

From these dimensions, the authors trace the geographic metaphors that recur in the literature. Food deserts describe areas where affordable, nutritious food is sparse and where distance and transportation barriers constrain access. Food swamps describe areas where fast-food restaurants and convenience stores predominate over supermarkets and produce markets, increasing exposure to ultra-processed foods and shifting dietary defaults toward products that are inexpensive per calorie but metabolically unfavorable. Food mirages highlight a subtler barrier: healthier outlets may be geographically proximate, yet their prices exceed the purchasing power of low-income households, making proximity without price feasibility functionally equivalent to constrained access. These constructs are not mutually exclusive, and the review emphasizes that such vulnerability patterns are not random but produced by structural forces, including residential segregation, economic disinvestment, and policy decisions, a phenomenon often described as food apartheid.

Measuring these environments is methodologically demanding, and the review catalogs the main approaches. Geographic information system-based spatial metrics quantify outlet density within buffer zones and proximity to the nearest retailer, using Euclidean, Haversine, Manhattan, or network distances, sometimes translated into estimated travel time. Retail audit tools such as the Nutrition Environment Measures Survey for stores and restaurants capture in-store availability, pricing, and quality. Retail food environment indices, including the CDC’s Modified Retail Food Environment Index, summarize the percentage of healthy retailers relative to total food retailers in an area. At broader scales, researchers draw on the USDA Food Environment Atlas and commercial datasets such as NielsenIQ retail scanner data, while diet quality linkage uses the Healthy Eating Index and food processing is classified with the NOVA framework, which sorts foods from unprocessed or minimally processed items to ultra-processed foods in group four.

These tools carry quantifiable weaknesses. Commercial business listings are marketing products rather than research instruments, and validation studies comparing them against ground-truthed field observations report substantial error. One field census found that Dun and Bradstreet undercounted 24 percent of existing supermarkets and grocery stores and InfoUSA 29 percent, with undercounts rising to 42 and 39 percent once errors in outlet-type classification were included. A meta-analysis of validation studies found wide variability in accuracy, with performance differing by population density and store type, and public directory sources have been shown to characterize food environments poorly in predominantly rural areas. The review also cautions that NOVA classifies foods by the nature, extent, and purpose of processing rather than nutrient composition alone, so ultra-processed foods represent a heterogeneous category that should not be interpreted as having uniform nutritional profiles, even though such foods account for roughly 42 to 60 percent of total dietary intake in many high-income countries.

The mechanistic core of the review links ultra-processed food consumption to cardiometabolic disease through interconnected metabolic, inflammatory, and vascular pathways. High-glycemic-index carbohydrates, prevalent in ultra-processed foods because of extensive refining and rapidly digestible sugars and starches, produce sharp postprandial increases in blood glucose and insulin, and repeated insulin dysregulation promotes insulin resistance, pancreatic beta-cell stress, and impaired glucose levels. Chronic hyperglycemia drives the formation of advanced glycation end products that injure vasculature and promote endothelial dysfunction, prothrombotic states, obesity, dyslipidemia, and hypertension, ultimately manifesting as type 2 diabetes, coronary artery disease, heart failure, cerebrovascular disease, chronic kidney disease, and peripheral arterial disease. Beyond caloric surplus, ultra-processed foods can disrupt gut microbiota composition, reduce microbial diversity, and increase intestinal permeability, allowing bacterial lipopolysaccharides to translocate into systemic circulation and activate inflammatory pathways that impair insulin signaling. Emulsifiers, common additives in these products, may directly disrupt the gut mucus layer and promote inflammatory responses independent of caloric intake, while microbial metabolites such as trimethylamine N-oxide and delta-valerobetaine have been linked to cardiovascular disease and obesity, respectively.

The epidemiologic evidence reviewed is substantial, though the authors stress that most of it remains observational and that dietary associations should not be read as direct causal evidence linking neighborhood food environments to clinical outcomes. In a large Canadian cross-sectional analysis using national nutrition survey data, individuals with the highest ultra-processed food intake, nearly three-quarters of total energy intake, had a 37 percent higher risk of diabetes than those with the lowest intake. In a large French cohort followed for approximately six years, higher ultra-processed food consumption was associated with incident type 2 diabetes independent of overall dietary quality. A UK cohort study demonstrated a dose-response relationship, with each 10 percent increase in ultra-processed food consumption associated with a 12 percent higher risk of type 2 diabetes, and individuals in the highest consumption group had a 44 percent greater risk over a median follow-up of 5.4 years. For cardiovascular disease, the French prospective cohort of 105,159 adults, using repeated 24-hour dietary records covering more than 3,300 food items, found higher ultra-processed food intake associated with increased incidence of overall cardiovascular disease, coronary artery disease, and cerebrovascular disease over a median follow-up of 5.2 years. In the Tehran Lipid and Glucose Study, a prospective cohort of 2,050 Iranian adults aged 30 and older without baseline cardiovascular disease, each 50-gram-per-day increase in ultra-processed food intake was associated with a 22 percent higher cardiovascular disease risk over 10.6 years, and the highest intake tertile carried a 68 percent greater risk than the lowest. An umbrella review spanning 14 meta-analyses and 9,888,373 participants found a direct association between greater ultra-processed food consumption and cardiovascular disease-related mortality, with a risk ratio of 1.50 and a 95 percent confidence interval of 1.37 to 1.63. For chronic kidney disease, a meta-analysis of observational studies reports roughly a 25 percent increased risk of incident disease with high ultra-processed food intake, with each 10 percent increase in intake corresponding to approximately a 7 percent greater risk, and among people with preexisting kidney disease, greater consumption is linked to faster progression and higher mortality.

A distinctive contribution of the review is its treatment of the food environment as one node in a web of interacting exposures. Walkable neighborhoods, characterized by connected street networks and mixed land use, translate proximity to healthy retail into better dietary quality, while car-dependent environments can undermine the benefits of healthy food availability, and evidence from built-environment studies suggests walkability modifies the association between food access and obesity, diabetes, and cardiovascular outcomes in a potentially synergistic rather than merely additive way. Air pollution, the leading environmental contributor to global morbidity and mortality with close to 10 million deaths each year worldwide, clusters within the same neighborhoods as unhealthy food environments, reflecting shared structural determinants such as industrial zoning, highway placement, and historical disinvestment, and some population studies suggest diets rich in antioxidants and fiber may blunt certain pollution-related cardiometabolic effects. Climate stressors add further layers: extreme heat disrupts agricultural productivity, food distribution, and pricing, shortens the shelf life of fresh produce in under-resourced stores, reduces income among heat-exposed workers, and shifts household consumption away from perishable nutrient-rich foods toward shelf-stable products, while spatial analyses show heat exposure, food insecurity, and neighborhood deprivation frequently cluster geographically.

Socioeconomic vulnerability and emerging exposures complete the picture. Historical practices such as redlining, discriminatory housing and lending policies, and exclusionary zoning have shaped present-day neighborhood environments, leaving historically disinvested areas more likely to lack supermarkets, host higher concentrations of fast-food outlets, and face greater exposure to air pollution and extreme heat. Chronic psychosocial stress linked to poverty and discrimination activates neuroendocrine and inflammatory pathways that promote visceral fat accumulation, insulin resistance, and elevated blood pressure. Meanwhile, ultra-processed foods are more likely than minimally processed foods to be packaged in plastic, raising the potential for ingestion of micro- and nanoplastics through food contact, storage, and heating, and experimental and toxicological studies suggest ingested microplastics may affect metabolic health through oxidative stress, endocrine disruption, gut microbiota alterations, and chronic low-grade inflammation, with dietary intake appearing to be a major route of exposure.

The authors are candid about the limits of the evidence base. Most research comes from North America, Western Europe, and other high-income settings, limiting generalizability to low- and middle-income countries, many of which face a double burden of undernutrition and diet-related chronic disease. Much of the literature is cross-sectional, exposure definitions are heterogeneous, and key biases such as selective migration, differential healthcare access, and unmeasured commercial determinants are often incompletely addressed, while static neighborhood boundaries may not reflect actual exposure for people whose daily activity spaces extend beyond home. The review calls for prospective designs with repeated exposure and outcome measurement, multi-country research networks using common geospatial approaches, integration of objective metrics with community-informed and person-centered assessments, and natural experiments evaluating retail activity, pricing policies, and nutrition assistance. Until that evidence matures, the authors position the food environment as a structural determinant whose modification, alongside parallel investments in pedestrian infrastructure and equity-focused policy, could meaningfully reduce cardiometabolic disease burden and the disparities that have persisted across generations.

Subject of Research: The food environment as a structural cardiometabolic exposure within the exposome framework

Article Title: The food environment as a cardiometabolic exposure: mechanisms, inequities, and interacting environmental risk

Article References: Vieira de Oliveira Salerno, P. R., Zhan, J., Estrada-Mendizabal, R. J., Aboukhatwa, O., Hum, A., Bassiony, M., Al Dakar, L., Setia, G., Freedman, D., Al-Kindi, S., Deo, S. V., & Dong, W. (2026). The food environment as a cardiometabolic exposure: mechanisms, inequities, and interacting environmental risk. Frontiers in Nutrition, 13, Article 1851911. https://doi.org/10.3389/fnut.2026.1851911

Image Credits: AI Generated

DOI: 10.3389/fnut.2026.1851911

Keywords: food environment, cardiometabolic risk, ultra-processed food, exposome, food insecurity, type 2 diabetes, cardiovascular disease, chronic kidney disease, food deserts, air pollution, walkability, health inequities